Highlights the high prevalence and mechanisms of LVH in CKD/ESRD and calls for new therapeutic paradigms to prevent and reverse cardiac fibrosis and hypertrophy in this population.
Chronic kidney disease (CKD) and ESRD, treated with conventional hemo- or peritoneal dialysis are both associated with a high prevalence of an increase in left ventricular mass (left ventricular hypertrophy LVH), intermyocardial cell fibrosis, and capillary loss. Cardiac magnetic resonance imaging is the best way to detect and quantify these abnormalities, but M-Mode and 2-D echocardiography can also be used if one recognizes their pitfalls. The mechanisms underlying these abnormalities in CKD and ESRD are diverse but involve afterload (arterial pressure and compliance), preload (intravascular volume and anemia), and a wide variety of afterload/preload independent factors. The hemodynamic, metabolic, cellular, and molecular mediators of myocardial hypertrophy, fibrosis, apoptosis, and capillary degeneration are increasingly well understood. These abnormalities predispose to sudden cardiac death, most likely by promotion of electrical instability and re-entry arrhythmias and congestive heart failure. Current treatment modalities for CKD and ESRD, including thrice weekly conventional hemodialysis and peritoneal dialysis and metabolic and anemia management regimens, do not adequately prevent or correct these abnormalities. A new paradigm of therapy for CKD and ESRD that places prevention and reversal of LVH and cardiac fibrosis as a high priority is needed. This will require novel approaches to management and controlled interventional trials to provide evidence to fuel the transition from old to new treatment strategies. In the meantime, key management principles designed to ameliorate LVH and its complications should become a routine part of the care of the patients with CKD and ESRD.
Glassock et al. (Tue,) studied this question.